Constrictive pericarditis is a condition characterized by decreased elasticity and an increased thickening of the double-layered sac surrounding the heart (pericardium).[2] These changes reduce the capacity of the heart to fill with blood and can lead to symptoms of heart failure.[2]
This condition can result from various disease processes which can have similar symptoms, and has been historically difficult to diagnose.[3] Understanding the differing etiologies and disease processes is important as it can lead to a timely diagnosis and appropriate treatment.[4]
Signs and symptoms
Constrictive pericarditis can present with symptoms such as difficulty breathing, fatigue, abdominal swelling, or swelling of legs.[2] Physical examination findings can include elevated Jugular venous pressure (JVP), Kussmaul's sign, Peripheral edema, Ascites, Hepatomegaly.[2] On auscultation a high-pitched sound heard during the early stage of diastole known as a pericardial knock may be appreciated. [5]
Causes
In areas of the world where Tuberculosis is endemic, it is the most common cause of constrictive pericarditis.[6] Outside of these areas the next most common cause is typically idiopathic or viral in nature.[4] Causes of constrictive pericarditis can include:
The pathophysiological characteristics of constrictive pericarditis are due to a thickened, fibrotic pericardium that forms a non-compliant shell around the heart. This shell prevents the heart from expanding when blood enters it. As pressure on the heart increases, the stroke volume decreases as a result of a reduction in the diastolic expansion in the chambers. [9] This results in significant respiratory variation in blood flow in the chambers of the heart.[10]
During inspiration, pressure in the thoracic cavity decreases but is not relayed to the left atrium which can lead to a reduced flow to the left atrium and ventricle. During diastole, less blood flow in the left ventricle allows for more room for filling in right ventricle and therefore a septal shift occurs.[11]
During expiration, the amount of blood entering the left ventricle will increase, allowing the interventricular septum to bulge towards the right ventricle, decreasing the right heart ventricular filing.[12]
Classification
Constrictive pericarditis can be categorized into general syndromes that reflect the nature of the disease development and course.[13]
Transient (subacute) constrictive pericarditis: constrictive pathophysiology may be reversible due to a transient inflammatory state that resolves without significant fibrosis.[4]
Advanced (chronic) constrictive pericarditis: constrictive pathophysiology may be irreversible due to significant fibrosis and loss of elasticity over a longer period of time (often 3-6 months).[4]
Effusive-constrictive pericarditis: similar yet distinct disease process to constrictive pericarditis characterized by a constrictive pathophysiology and the presence of a pericardial effusion.[4]
Diagnosis
Tuberculosis-x-ray
The diagnosis of constrictive pericarditis is often difficult to make. In particular, restrictive cardiomyopathy has many similar clinical features to constrictive pericarditis, and differentiating them in a particular individual is often a diagnostic dilemma.[14]
Chest X-Ray - pericardial calcification (common but not specific), pleural effusions are common findings.[15]
Echocardiography - the principal echographic finding is changes in cardiac chamber volume.[15]
CT and MRI - CT scan is useful in assessing the thickness of pericardium, calcification, and ventricular contour. Cardiac MRI may find pericardial thickening and pericardial-myocardial adherence. Ventricular septum shift during breathing can also be found using cardiac MRI. Late gadolinium enhancement can show enhancement of the pericardium due to fibroblast proliferation and neovascularization.[12]
BNP blood test - tests for the existence of the cardiac hormone brain natriuretic peptide, which is only present in restrictive cardiomyopathy but not in constrictive pericarditis[16]
Physical examination - can reveal clinical features including Kussmaul's sign and a pericardial knock.[17]
X-ray demonstrating constrictive pericarditis with calcifications.
Treatment and Prognosis
Pericardium visualized in open heart surgery
Transient or subacute constrictive pericarditis is treated with anti-inflammatory medication and can resolve without surgical intervention in many cases.[4] Cases that do not resolve with medication may be treated similar to chronic constrictive cases which often require surgical intervention.[4] In these cases the outcome of surgery may be improved as the pericardial inflammation would be decreased due to the medication trial.[4]
The definitive treatment for advanced or chronic constrictive pericarditis is a radical Pericardiectomy, which is a surgical procedure in which the entire pericardium is peeled away from the heart. This procedure has significant risk involved,[18] with mortality rates of 6% or higher in major referral centers.[19]
A poor outcome is often the result after a pericardiectomy is performed for radiation-induced constrictive pericarditis, and some patients may develop heart failure post-operatively.[20]
Epidemiology
Constrictive pericarditis is a rare complication of many pericardial diseases.[13] It seen as a complication in approximately 1% of idiopathic pericarditis cases, and even fewer cases post cardiac surgery.[13]
The geographic distribution of constrictive pericarditis can be categorized based on etiology, with idiopathic or viral pericarditis considered to be the leading cause in Western countries.[13]In Western countries the remaining causes tend to be post-surgical, post-radiation, infectious, and connective tissue disorders.[13] In some developing countries Tuberculosis has been noted as the leading cause of constrictive pericarditis.[6]
↑Cinar B, Enc Y, Goksel O, Cimen S, Ketenci B, Teskin O, Kutlu H, Eren E (2006). "Chronic constrictive tuberculous pericarditis: risk factors and outcome of pericardiectomy". Int J Tuberc Lung Dis. 10 (6): 701–6. PMID16776460.
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